الفهرس 
Introduction and aim of the workOnly 14 pages are availabe for public view
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Abstract
Psoriasis, lichen planus (LP), and atopic dermatitis are common chronic inflammatory skin diseases . The exact pathogenesis of these diseases until now is not fully determined. They may result from complex interactions of innate and adaptive immune responses based on a strong genetic predisposition and triggered by environmental factors.
Recently, Th17 cells (IL-17-producing CD4+ T cells) have been discovered as a unique subset of T helper cells that develop along a pathway that is distinct from the Th1 and Th2 differentiation pathways. Th17 cells are characterized by the production of the potent proinflammatory cytokines IL17, IL17F, IL21, IL22 and IL26. The presence of Th17 cells and their signature cytokine, IL17, has been demonstrated in autoimmune pathology, infectious inflammatory states and tumour microenvironments.
IL23 is a key cytokine in bridging the innate and adaptive arms of the immune response . IL23 possesses unique immunological properties such as its ability to differentiate/expand memory T cells, regulate proliferation of Th17 cells and increase production of IL17.
Although it is becoming evident that many Th1 diseases including psoriasis have a strong IL17 signal, the importance of the Th17 cells in AD and lichen planus is still unclear, leading us to investigate its role in these diseases, as compared with psoriasis. This study aimed at the detection of serum interleukin 23 and interleukin 17 in psoriasis, lichen planus and atopic dermatitis, and whether these interleukins could be candidate biomarkers of the diseases activity.
A total of sixty adult patients were included in this study; they were divided into 3 groups, 20 patients each, of psoriasis, atopic dermatitis and lichen planus (13 patients with combined cutaneous and oral lp and 7 patients with cutaneous lp only), 8 of lichen planus patients were HCV positive. In addition to twenty healthy subjects taken as control. The activity of the diseases was estimated at the time of examination using specific activity index for each disease. The serum levels of IL23 and IL17A had been estimated by ELISA.
It has been found that these diseases had significantly higher serum levels of IL17A and IL23 than the control group. The serum levels of both interleukins were higher in psoriasis compared with lichen planus and atopic dermatitis, but the difference between psoriasis and lichen planus was not statistically significant. There was no correlation between the serum levels of IL23, IL17 and the clinical severity of the three diseases. On the other hand, a significant positive correlation between IL23 and IL17was found in the three groups of patients.
As regard lichen planus, patients who had both cutaneous and oral LP had significantly higher serum levels of IL23 and IL-17 than patients of cutaneous LP only . Meanwhile, there was no significant difference of the serum levels of IL23 and IL-17 between HCV positive and HCV negative patients .
In conclusion, our findings demonstrated that IL23 and IL17 may play a role in the pathogenesis of the three diseases but not the maestro in controlling these diseases and cannot be used as a marker of their severity. On the other hand , the significant positive correlation between IL23 and IL17in the three diseases confirm that IL23 is important for IL17 production and suggest that the factors affect IL23 will be reflected on IL17 levels.
Recommendations:
Future studies are recommended on a larger number of patients with correlation of the serum level of IL23 and IL17 with their expression pattern in the skin lesions for better understanding of their exact pathogeneic role in the immunopathogenesis of these diseases.